Dr. Andreas Eenfeldt response:

http://www.dietdoctor.com/calorie-t...esity-falsified

I liked Eenfeldt response better than Eades (obviously).

The odd thing in the study is that EE and RE increased a small but measurable bit. Calories were constant. Weight loss slowed. Wait, what? If calories are constant, expenditures are going up then there should have been higher weight loss not lower.

Again though, I really doubt the ability to measure this stuff very accurately.

I'd like to point out something about hormones. They are received by cells through receptors, and cells can open and close those receptors, and/or respond more or less to those hormones for various reasons.

So, here it's the idea of signaling, rather than absolute hormone level. Cells can maintain the same response by closing and opening receptors, in spite of fluctuating hormone level. And, cells can modulate their response, in spite of constant hormone level.

Take the liver and insulin for example. The liver is where insulin is degraded primarily, therefore merely by modulating insulin receptors, the liver can cause insulin level to rise and drop, which in turn will have an effect on all other tissue, and then all these other tissues can modulate their insulin receptors. This will happen even if the pancreas produces a constant quantity of insulin.

Or the testes. They produce a relatively constant quantity of T, while various tissues open and close T receptors (or activate the various internal enzymes to respond), following exertion from a workout. GH, same. Leptin, same. Ghrelin, epinephrine, T3, etc, all the same principle.

In the case of insulin and fat tissue, there's a phenomenon called insulin-induced lipohypertrophy. It occurs when insulin remains high for long periods, fat tissue actually grows bigger permanently. If this happened instantly and/or quickly, we'd be forever growing fatter. Fat tissue can grow and shrink quickly, temporarily. It must, otherwise we couldn't store fuel, we couldn't release fuel on demand. It must do this, but it must also resist growing bigger permanently. So, first, fat tissue has a tremendous capacity to store fat, and second, it can shut down insulin receptors when it's overfull. At this point, something happens. Fat cells somehow stop responding to insulin, but fat tissue grows bigger permanently. So there's other cells that now respond to insulin (probably pre-adipocytes, through a process called proliferation), suggesting they opened up their insulin receptors.

As we can see, every cell has the ability to modulate their response to hormones. Once we figure out how that works for obesity, we'll be able to quantify and predict fat tissue size, growth, and shrinkage. We'll also be able to quantify and predict subsequent effect on Ein and Eout, and the opposite effect of fluctuating Ein and Eout on hormone levels and response of various tissues.

Incidentally, the whole thing falls within the carb/insulin hypothesis, which I'm going to rename the hormone/receptor hypothesis, cuz it's just more representative of what's really going on, and honestly what genuine scientist is gonna argue against that.

Here's another interesting idea. Mechanistic versus end-point causality. In this experiment, it's a bit of both. They tested whether the end-points (diet -> weight/fat) are causally linked through a specific mechanism (insulin). Now here's a question. What is the mechanism of calories? It's an absurd question. There is no such mechanism. So, regardless of whether they confirmed or refuted the carb/insulin hypothesis, they cannot possibly confirm nor refute the calorie hypothesis, because they cannot point to a specific calories mechanism. In effect, the calorie hypothesis is untestable.

Even if it was testable, the nature of the First Law is such that there's absolutely no room for even a single atom to disappear or appear from/into our reality, let alone 100kcals.

I think Attia was on to something with his fat flux model. It is mathematically correct while being simple enough to build upon. Add a liver flux, pancreas flux, muscle flux model, stomach flux model, large intestine flux model and now we are talking.


Not one iota of room. Energy is neither created nor destroyed. It goes somewhere. We just have to figure out where.

Peter at Hyperlipid response: http://high-fat-nutrition.blogspot....eight-loss.html

Peter is too techie for me. But I like this: Seems like that takes in something of the complexity we all experience, with or without a scientific explanation.

This leaves room for interesting speculation. You'd think--it takes less calories to produce the ATP to walk a mile at a certain speed. Then you look at anecdotes where people go on a low carb diet, and they find that they have more energy to go about their daily tasks, even before they've lost very much weight. Usually put down to easier access to energy--but more efficient use of calories to produce ATP might fit the bill.

Less calories being burned in exercise, or just standing still, neither is really a disadvantage, if a person ends up twitchy and active enough to make up the difference.

Some ketomice do get fat on keto--even if their bodyweight is lower than control mice, they can be considerably fatter by percent bodyweight. Given access to voluntary exercise on a running wheel, they lose the excess fat--it's not calories burned on the running wheel, or not just, they also end up eating less--almost as if exercise-induced lipolysis was helping to satisfy their appetite. *cough*

Peter is conflating VO2 with being exclusively equivalent to calories burned. The problem with that is that (as Peter mentions) the hydrogen to carbon ratio of the fuel source changes as one changes from carbs to fat. What he doesn't get is that VO2, VCO2 and VH2O change. Exercise scientists use VO2 as a surrogate for the others but that only works when the fuel source remains the same. Moreover VO2 is not just constrained by lung capacity but also heart capacity (it is almost practically impossible for them to be different). That heart capacity is the lesser of the sending vs. receiving capacity of the heart. IOW if the venous side of the heart has a capacity of 10lpm and the arterial side has a capacity of 9lpm then the heart has a capacity of 9lpm. If the lungs can process 11lpm of keto blood an 9lpm of carb-blood then the fundamentals of all the calculations are off and have to be recalculated from first principles.

Have I worked it all out on paper for everyone to use? No and I feel that. I need to but I have not.

Why do they all seem to be ignoring the role of stored fat? As we lose weight with low carb, isn't that where new energy should come from? As it is liberated and metabolized?

Dr David Ludwig responds:

https://medium.com/~davidludwigmd/d...7257#.t36ypql9r

Richard David Feinman's response:

https://feinmantheother.com/2016/05...teral-estoppel/

Introductory Paragraph:

Sorry, Rob. In this short excerpt, I'm not sure I understand what Feinman is saying. That there's no such thing as one diet or another that "works better" for weight loss? That the number of calories consumed DOES matter, no matter what diet you use?

I don't think that's what he's saying quite. Saying that most people's bodies, most of the time, will produce atp with roughly the same efficiency, from the same calories as fat or as glucose, doesn't deny the fattening hormonal effects of elevation of insulin, or the very different effects on appetite that different dietary approaches will have. The body has mechanisms to make metabolism more or less efficient for atp production as well as I guess heat production, there are homeostatic mechanisms to keep both of these within certain ranges. And he leaves things open for individual variation, for black swans, people who don't fit into the general rule.

That's Feinman's point in addition to his contention that there's no longer the need to spend time discussing/studying/researching CICO diet theory as if it had merit. He lists several ways that the first law of thermodynamics is not applicable to the human metabolism. He goes into far more detail in his book, "The World Turned Upside Down," for those who desire a more rigorous explanation.

What's also interesting are the varied reviews of Hall's study where some focus on his comments on ketosis and others focus on CICO. Feinman focuses strictly on the CICO findings. I saw a comment from Dr. Fung that he plans to weigh in on NuSI Hall in an upcoming blog. Should be interesting . . .

Sorry, in my first post, I included a copy of the Introductory paragraph, but meant for all to read Feinman's full blog post. Here's some more, but the full post in easily accessible: